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Cells
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Cellular and Molecular Mechanisms in Bone and Cartilage Damage and...
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Cellular and Molecular Mechanisms in Bone and Cartilage Damage and Regeneration

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 28 February 2025 | Viewed by 1850

Special Issue Editor

Prof. Dr. Philippe Hernigou

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Guest Editor
Orthopaedic Surgery, University Paris East (UPEC), 94010 Creteil, France
Interests: cell therapy; bone union; cartilage regeneration; osteonecrosis

Special Issue Information

Dear Colleagues,

Bones and cartilage, the two most important parts of the musculoskeletal system, provide mobility and maintain the body’s posture. Bone and cartilage damage can have a highly deleterious impact on life and society; therefore, understanding the mechanisms of bone and cartilage regeneration is important. However, questions remain regarding the precise mechanisms of bone formation, how the different molecular processes interact, and the real identity of regenerative cells. 

In this Special Issue, we invite researchers and industry experts to submit their original research articles and reviews related to the following topics and keywords: 

Bone Morphogenic Proteins (BMPs): The role of BMPs in bone and cartilage regeneration; BMP signaling pathways and their implications in orthopedic therapies; and innovative uses of BMPs in reconstructive surgery.

Bone Union with Cell Therapy: Advances in stem cell therapies for fracture non-union; mechanisms and applications of mesenchymal stem cells (MSCs) in bone healing; comparative studies on bone marrow-derived MSCs versus expanded MSCs; and the role of endothelial progenitor cells (EPCs) in bone regeneration.

Cartilage Regeneration: novel cell-based therapies for cartilage repair; functional of collagen/PLA scaffolds in cartilage regeneration; and BMPs in regulating inflammation and promoting osteogenesis at injured growth plates.

Regeneration and Revascularization of Bone Osteonecrosis: Evaluation of bone turnover markers in MSC-regenerative approaches for osteonecrosis; research studies and reviews in bone regeneration for osteonecrosis patients; and evaluation of osteonecrosis regeneration with MRI and histology, and arteriography.

Cartilage Biomarkers: The identification and validation of new cartilage biomarkers; biomarkers in monitoring the progress of cartilage regeneration therapies; and the role of biochemical markers in the diagnosis and treatment of cartilage damage.

Diaphyseal Regeneration with Callostasis: Techniques and outcomes of callostasis in diaphyseal bone regeneration; the use of BMPs and cell-based therapies in enhancing callostasis; and research studies and reviews on the SECCS system and other scaffold-based therapies.

Union with the Membrane Technique: Advances in the membrane technique for guided bone regeneration; mechanisms and applications of barrier membranes in bone healing; and combination therapies involving BMPs and membranes for optimal bone regeneration.

Submissions should provide novel insights, comprehensive reviews, or significant advancements in the field of bone and cartilage damage and regeneration. We hope that a better understanding of the underlying mechanisms can facilitate the development of new strategies for improving bone and cartilage regeneration.

Prof. Dr. Philippe Hernigou
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • bone morphogenic proteins (BMPs)
  • bone union with cell therapy
  • advances in stem cell therapies for fracture non-union and cartilage regeneration
  • novel cell-based therapies for cartilage repair
  • functional of collagen/PLA scaffolds in cartilage regeneration
  • regeneration and revascularization of bone osteonecrosis
  • evaluation of osteonecrosis regeneration with MRI and histology, and arteriography
  • identification and validation of new cartilage biomarkers
  • diaphyseal regeneration with callostasis
  • union with the membrane technique

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

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23 pages, 7484 KiB  
Article
Unraveling the Mechanism of Impaired Osteogenic Differentiation in Osteoporosis: Insights from ADRB2 Gene Polymorphism
by Olga Krasnova, Julia Sopova, Anastasiia Kovaleva, Polina Semenova, Anna Zhuk, Daria Smirnova, Daria Perepletchikova, Olga Bystrova, Marina Martynova, Vitaly Karelkin, Olga Lesnyak and Irina Neganova
Cells 2024, 13(24), 2110; https://doi.org/10.3390/cells13242110 - 20 Dec 2024
Viewed by 276
Abstract
Osteoporosis is characterized by increased resorption and decreased bone formation; it is predominantly influenced by genetic factors. G-protein coupled receptors (GPCRs) play a vital role in bone homeostasis, and mutations in these genes are associated with osteoporosis. This study aimed to investigate the [...] Read more.
Osteoporosis is characterized by increased resorption and decreased bone formation; it is predominantly influenced by genetic factors. G-protein coupled receptors (GPCRs) play a vital role in bone homeostasis, and mutations in these genes are associated with osteoporosis. This study aimed to investigate the impact of single nucleotide polymorphism (SNP) rs1042713 in the ADRB2 gene, encoding the beta-2-adrenergic receptor, on osteoblastogenesis. Herein, using quantitative polymerase chain reaction, western immunoblotting, immunofluorescence assays, and flow cytometry, we examined the expression of ADRB2 and markers of bone matrix synthesis in mesenchymal stem cells (MSCs) derived from osteoporosis patient (OP-MSCs) carrying ADRB2 SNP in comparison with MSCs from healthy donor (HD-MSCs). The results showed significantly reduced ADRB2 expression in OP-MSCs at both the mRNA and protein levels, alongside decreased type 1 collagen expression, a key bone matrix component. Notably, OP-MSCs exhibited increased ERK kinase expression during differentiation, indicating sustained cell cycle progression, unlike that going to HD-MSC. These results provide novel insights into the association of ADRB2 gene polymorphisms with osteogenic differentiation. The preserved proliferative activity of OP-MSCs with rs1042713 in ADRB2 contributes to their inability to undergo effective osteogenic differentiation. This research suggests that targeting genetic factors may offer new therapeutic strategies to mitigate osteoporosis progression. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Bone and Cartilage Damage and Regeneration)
►▼ Show Figures

Figure 1

Figure 1
<p>The morphology and phenotype of cells derived from the healthy donor’s and the osteoporotic patient’s bone samples. (<b>A</b>) Phase contrast representative image of cells derived from bone samples of a healthy donor and (<b>A’</b>) image of cells derived from bone samples of an osteoporotic patient; scale bar 400 μm. (<b>B</b>) Immunophenotype of cells derived from bone samples of a healthy donor and (<b>B’</b>) cells derived from bone samples of an osteoporotic patient. Cells are positive for mesenchymal stem cell markers CD90, CD105, and CD73, while they are negative for CD34 and CD45 blood cell markers.</p> Full article ">Figure 2
<p>Expression of the beta-2-adrenergic receptor (ADRB2) in MSCs from the healthy donor and the osteoporotic patient bone samples. (<b>A</b>) Immunofluorescence analysis of ADRB2 expression in MSCs derived from the healthy donor’s bone samples (HD-MSCs) and (<b>A’</b>) MSCs from the osteoporotic patient’s bone samples (OP-MSCs), cultured in basal medium or osteogenic medium within 14 days; scale bar 50 μm. Abbreviations: ADRB2—beta-2-adrenergic receptor and DAPI—4′,6-diamidino-2-phenylindole. (<b>B</b>) Electron microscopy observation of ADRB2 in HD-MSCs and (<b>B’</b>) OP-MSCs cultured in basal or osteogenic media for 14 days; scale bar 1 μm. Red frames and arrows point at ADRB2 on cell membrane. Red asterisks point at ADRB2 within cells, distinct from the membrane. (<b>C</b>) Relative ADRB2 intensity in HD-MSCs and OP-MSCs cultured in the basal medium and osteogenic medium. Data are shown as mean ± SD, <span class="html-italic">n</span> &gt; 8, with the significant differences indicated with asterisks (ns—not significant, *—<span class="html-italic">p</span> &lt; 0.05). (<b>D</b>) The mRNA level of <span class="html-italic">ADRB2</span> in HD-MSCs and OP-MSCs under the basal medium or osteogenic medium conditions. Data are shown as mean ± SD, <span class="html-italic">n</span> = 3, with significant differences indicated with asterisks (ns—not significant, **—<span class="html-italic">p</span> &lt; 0.01, ***—<span class="html-italic">p</span> &lt; 0.001, ****—<span class="html-italic">p</span> &lt; 0.0001). Abbreviations: HD—healthy donor, OP—osteoporotic patient, BM—basal medium, OM—osteogenic medium, and GAPDH—glyceraldehyde 3-phosphate dehydrogenase. (<b>E</b>) Western blot analysis of ADRB2 expression (<b>E’</b>) and the relative ADRB2 protein level in HD-MSCs and in OP-MSCs cultured in the basal medium and osteogenic medium. Full-length blots are presented in <a href="#app1-cells-13-02110" class="html-app">Supplementary Figure S1A,B</a>. Data are shown as mean ± SD, <span class="html-italic">n</span> = 3, with significant differences indicated with asterisks (**—<span class="html-italic">p</span> &lt; 0.01, ***—<span class="html-italic">p</span> &lt; 0.001, ****—<span class="html-italic">p</span> &lt; 0.0001). (<b>F</b>) <span class="html-italic">RANKL</span> gene expression in HD-MSCs and in OP-MSCs under the basal medium and osteogenic medium conditions. Data are shown as mean ± SD, <span class="html-italic">n</span> = 3, with the significant difference indicated with asterisks (****—<span class="html-italic">p</span> &lt; 0.0001).</p> Full article ">Figure 3
<p>Osteogenic differentiation of HD-MSCs and OP-MSCs. (<b>A</b>,<b>A’</b>) <span class="html-italic">RUNX2</span>, <span class="html-italic">COL1A1</span>, <span class="html-italic">SP7</span>, <span class="html-italic">POSTN</span>, <span class="html-italic">ATF4</span>, and <span class="html-italic">BGLAP</span> gene expression in HD-MSCs and OP-MSCs after 7 days of osteogenic differentiation. Data are shown as mean ± SD, <span class="html-italic">n</span> = 3, with significant differences indicated with asterisks (ns—not significant, *—<span class="html-italic">p</span> &lt; 0.05, ***—<span class="html-italic">p</span> &lt; 0.001, ****—<span class="html-italic">p</span> &lt; 0.0001). (<b>B</b>,<b>B’</b>) ALP activity after 14 days of osteogenic differentiation of HD-MSCs and OP-MSCs. (<b>C</b>,<b>C’</b>) Alizarin Red staining after 21 days of osteogenic differentiation of HD-MSCs and OP-MSCs. (<b>D</b>) mRNA level of <span class="html-italic">FN1</span>, <span class="html-italic">SPARC</span>, <span class="html-italic">CAD11</span>, and <span class="html-italic">FNDC3B</span> after the osteogenic differentiation of HD-MSCs and OP-MSCs. Abbreviations: HD—HD-MSCs; OP—OP-MSCs. Data are shown as mean ± SD, <span class="html-italic">n</span> = 3, with significant differences indicated with asterisks (ns—not significant, *—<span class="html-italic">p</span> &lt; 0.05, ***—<span class="html-italic">p</span> &lt; 0.001, ****—<span class="html-italic">p</span> &lt; 0.0001).</p> Full article ">Figure 4
<p>Analysis of collagen type 1 expression. (<b>A</b>) Immunofluorescence analysis of RUNX2 (488 nm—green) and COL1A1 (561 nm—red) expression in HD-MSCs and (<b>A’</b>) OP-MSCs cultured in the basal medium and osteogenic medium for 14 days; scale bar 50 μm. Yellow frames point at RUNX2-positive and COL1A1-positive cells, which are shown at higher magnification in yellow insets. Yellow arrows point at RUNX2-positive cells; Abbreviations: DAPI—4′,6-diamidino-2-phenylindole. (<b>B</b>) relative intensity of RUNX2 and (<b>B’</b>) of COL1A1 in HD-MSCs and OP-MSCs cultured in the basal medium and osteogenic medium for 14 days. Data are shown as mean ± SD, <span class="html-italic">n</span> &gt; 8, with significant differences indicated with asterisks (ns—not significant, **—<span class="html-italic">p</span> &lt; 0.01, ****—<span class="html-italic">p</span> &lt; 0.0001). Abbreviations: HD—HD-MSCs; OP—OP-MSCs. (<b>C</b>) Western blot analysis of COL1A1 expression and (<b>C’</b>) relative COL1A1 protein level in HD-MSCs and OP-MSCs cultured in the basal medium and osteogenic medium for 14 days. Full-length blots are presented in <a href="#app1-cells-13-02110" class="html-app">Supplementary Figure S1C,D</a>. Statistical analysis of Western blot is represented in <a href="#app1-cells-13-02110" class="html-app">Supplementary Figure S2</a>. Data are shown as mean ± SD, <span class="html-italic">n</span> = 3, with significant difference indicated with asterisks (*—<span class="html-italic">p</span> &lt; 0.05, **—<span class="html-italic">p</span> &lt; 0.01, ***—<span class="html-italic">p</span> &lt; 0.001, ****—<span class="html-italic">p</span> &lt; 0.0001). Abbreviations: HD—HD-MSCs; OP—OP-MSCs. BM—basal medium; OM—osteogenic medium.</p> Full article ">Figure 5
<p>Expression of the beta-2-adrenergic receptor downstream targets and evaluating proliferation-related markers. (<b>A</b>) Expression of <span class="html-italic">GNAS</span>, <span class="html-italic">GNAI1</span>, <span class="html-italic">GNAI2</span>, and <span class="html-italic">GNAI3</span> genes in HD-MSCs and (<b>A’</b>) in OP-MSCs after osteogenic differentiation induction. Data are shown as mean ± SD, <span class="html-italic">n</span> = 3, with significant differences indicated with asterisks (ns—not significant, *—<span class="html-italic">p</span> &lt; 0.05, **—<span class="html-italic">p</span> &lt; 0.01 and ****—<span class="html-italic">p</span> &lt; 0.0001). (<b>B</b>) Simplified scheme of ADRB2 signaling. (<b>C</b>) Western blot analysis of phospho-CREB1 (Ser133), total CREB1, phospho-ERK1/2 (Thr202/Tyr204), total ERK1/2 in HD-MSCs, and OP-MSCs cultured in the basal medium and the osteogenic medium for 14 days. Abbreviations: BM—basal medium; OM—osteogenic medium; p—phosphorylated; t—total. (<b>D</b>) Cell cycle phase distribution of HD-MSCs and (<b>D’</b>) cultured in the basal medium and the osteogenic medium for 7 days. (<b>E</b>) Western blot analysis of Cyclin A and Cyclin B1 expression in HD-MSCs and OP-MSCs cultured in the basal medium and the osteogenic medium for 14 days. Full-length blots are presented in the Figure(s) 1E–L. Abbreviations: BM—basal medium; OM—osteogenic medium. (<b>F</b>) The mRNA level of <span class="html-italic">CCNA1</span> in HD-MSCs and in OP-MSCs after osteogenic differentiation. Data are shown as mean ± SD, <span class="html-italic">n</span> = 3, with significant differences indicated with asterisks (***—<span class="html-italic">p</span> &lt; 0.001). Abbreviations: BM—basal medium; OM—osteogenic medium.</p> Full article ">Figure 6
<p>The impact of propranolol treatment during osteogenic differentiation. (<b>A</b>) Cell cycle phase distribution of HD-MSCs and (<b>A’</b>) OP-MSCs cultured in the basal medium and the osteogenic medium with propranolol (10 μM) for 7 days. (<b>B</b>) Immunofluorescence analysis of COL1A1 (561 nm – red) expression in HD-MSCs and (<b>B’</b>) OP-MSCs cultured in the basal medium and the osteogenic medium, vehicle or propranolol (10 μM), for 14 days; scale bar 50 μm. Abbreviations: DAPI—4′,6-diamidino-2-phenylindole. (<b>C</b>) Relative COL1A1 intensity in HD-MSCs and OP-MSCs cultured in the basal medium and the osteogenic medium, vehicle or supplemented with propranolol (10 μM), for 14 days. Data are shown as mean ± SD, <span class="html-italic">n</span> &gt; 8, with the significant difference indicated with asterisks (ns—not significant, **—<span class="html-italic">p</span> &lt; 0.01). (<b>D</b>) Alizarin Red staining after 21 days of osteogenic differentiation, vehicle or with propranolol (10 μM) treatment of HD-MSCs and OP-MSCs. Abbreviations: BM—basal medium; OM—osteogenic medium; Veh—vehicle; PRO—propranolol.</p> Full article ">
14 pages, 3528 KiB  
Article
Therapeutic Potential of Stearoyl-CoA Desaturase1 (SCD1) in Modulating the Effects of Fatty Acids on Osteoporosis
by Young-Jin Seo, Jin-Ho Park and June-Ho Byun
Cells 2024, 13(21), 1781; https://doi.org/10.3390/cells13211781 - 28 Oct 2024
Viewed by 1043
Abstract
Osteoporosis is a common skeletal disease, primarily associated with aging, that results from decreased bone density and bone volume. This reduction significantly increases the risk of fractures in osteoporosis patients compared to individuals with normal bone density. Additionally, the bone regeneration process in [...] Read more.
Osteoporosis is a common skeletal disease, primarily associated with aging, that results from decreased bone density and bone volume. This reduction significantly increases the risk of fractures in osteoporosis patients compared to individuals with normal bone density. Additionally, the bone regeneration process in these patients is slow, making complete healing difficult. Along with the decline in bone volume and density, osteoporosis is characterized by an increase in marrow adipose tissue (MAT), which is fat within the bone. In this altered bone microenvironment, osteoblasts are influenced by various factors secreted by adipocytes. Notably, saturated fatty acids promote osteoclast activity, inhibit osteoblast differentiation, and induce apoptosis, further reducing osteoblast formation. In contrast, monounsaturated fatty acids inhibit osteoclast formation and mitigate the apoptosis caused by saturated fatty acids. Leveraging these properties, we aimed to investigate the effects of overexpressing stearoyl-CoA desaturase 1 (SCD1), an enzyme that converts saturated fatty acids into monounsaturated fatty acids, on osteogenic differentiation and bone regeneration in both in vivo and in vitro models. Through this novel approach, we seek to develop a stem cell-based therapeutic strategy that harnesses SCD1 to improve bone regeneration in the adipocyte-rich osteoporotic environment. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Bone and Cartilage Damage and Regeneration)
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Figure 1

Figure 1
<p>Schematic diagram illustrating the research concept. In osteoporosis models, fatty acids such as SFA and MUFA are secreted from expanding MAT. This study suggests that SCD1 can promote bone regeneration by converting SFA, which is known to have a negative effect on osteoblast differentiation and MSC proliferation, into MUFA, which can have a positive effect on bone metabolism. This highlights the therapeutic potential of MSCs through SCD1 overexpression in bone regeneration in osteoporosis models.</p> Full article ">Figure 2
<p>Evaluation of osteoporosis modeling in rats. (<b>A</b>) Schematic diagram of OVX surgery. (<b>B</b>) μCT images of femurs in the Sham and OVX groups. (<b>C</b>) Body weight (g). (<b>D</b>) Bone mineral density (BMD, g/cm<sup>2</sup>). (<b>E</b>) Bone volume fraction per total volume (BV/TV, %). (<b>F</b>) Histological examination of femoral bone marrow using H&amp;E staining. (<b>G</b>) Quantification of fat volume fraction per total volume (FV/TV, %). (<b>H</b>) Immunostaining for CD36 in the distal femur and cancellous bone. (* <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001).</p> Full article ">Figure 3
<p>Characterization of BM-MSCs. (<b>A</b>) CD marker analysis by flow cytometry; MSC markers (CD29 and CD90), hematopoietic cell markers (CD34 and CD45). (<b>B</b>) Evaluation of osteoblast differentiation by ALP staining and ARS staining, and evaluation of adipocyte differentiation by ORO staining.</p> Full article ">Figure 4
<p>Effect of adipocytes on osteoblast differentiation. (<b>A</b>) Schematic representation of the co-culture experiment. (<b>B</b>) ALP and ARS staining on days 10 and 20 after co-culture. (<b>C</b>) Evaluation of cell viability at different concentrations of palmitic acid. (<b>D</b>) Evaluation of palmitic acid concentration-dependent osteogenic differentiation by ALP and ARS staining. (<b>E</b>) Evaluation of the degree of osteogenic differentiation by calcium content measurement. (* <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.001).</p> Full article ">Figure 5
<p>Effect of SCD1 overexpression on osteogenic differentiation reduced by palmitic acid (PA). (<b>A</b>) Production of adenovirus-based SCD1 vector. (<b>B</b>) Confirmation of cell viability of BM-MSCs according to virus MOI. (<b>C</b>) Verification of MOI-dependent overexpression of Ad-SCD1. (<b>D</b>) Confirmation of normal virus infection and GFP expression in BM-MSCs. (<b>E</b>) Measurement of cell viability with the virus. (<b>F</b>–<b>I</b>) Confirmation of the effect of Ad-SCD1 on osteogenic differentiation of PA-treated BM-MSCs through comparison of ALP and ARS staining, ALP activity, and calcium deposition. (*** <span class="html-italic">p</span> &lt; 0.001).</p> Full article ">Figure 6
<p>In vivo experiments to verify the effect of SCD1 on bone defect recovery in an osteoporosis model. (<b>A</b>) Schematic diagram of the animal modeling experiment. (<b>B</b>) X-ray scan images of the left distal femur at 1, 3, 5, and 7 weeks after cell transplantation into the defect. (<b>C</b>) BMD measurements by DEXA imaging at 1, 3, 5, and 7 weeks (* <span class="html-italic">p</span> &lt; 0.05, *** <span class="html-italic">p</span> &lt; 0.001).</p> Full article ">
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Comparison of fresh and frozen bone marrow aspirate concentrate cells (BMAC) derived MSCs for in vitro multipotent differentiation and cartilage regeneration in rat OA model
Authors: Xueqin Gao
Affiliation: Steadman Philippon Research Institute (Fort Collins Lab), USA

Title: ACTIVATED CARBON FIBER INCORPORATED WITH METAL IONS: evaluation of biological bone interactions in vitro
Authors: Letícia Cavassini Torquato; Luiz Augusto Rodrigues Santos; Nátaly Domingues Almeida; Clarissa Carvalho Martins Maciel; Glenda Biasotto; Camilla Magnoni Moretto Nunes; Luana Marotta Reis de Vasconcellos; Jossano Saldanha Marcuzzo; Eduardo José de Arruda; Andrea Carvalho De Marco
Affiliation: São Paulo State University (UNESP)
Abstract: The present study had as main objective to evaluate the carbon fiber obtained from textile PAN fiber, in the different forms of presentation: non-activated carbon fiber felt (NACF) and activated carbon fiber felt (ACF) with silver (Ag-ACF), gold (Au-ACF), copper (Cu-ACF), palladium (Pd-ACF) and platinum (Pt-ACF), in the cellular behavior and osteogenesis of mesenchymal cells. Were assessed, cell proliferation, cell viability, quantification of calcium in mineralization nodules, total protein content and alkaline phosphatase activity were quantified, cell interaction by Scanning Electron Microscopy and genotoxicity. All samples were similar in terms of cell proliferation, except for the Ag-ACF group compared to the control group (C). Regarding cell viability, C obtained higher viability than the other groups, and ACF was superior to the Ag-ACF, Cu-ACF, Pt-ACF, being statistically similar to the Au-ACF and Pd-ACF groups. The Au-ACF and Pd-ACF groups presented statistically significant difference to the Ag-ACF and Cu-ACF groups. In the total protein expression Au-ACF had lower expression. For the alkaline phosphatase activity, the Ag-ACF and Cu-ACF showed inferior results. Au-ACF and Pd-ACF have demonstrated potential for future application as scaffolds for bone repair.

Title: Unraveling the mechanism of impaired osteogenic differentiation in osteoporosis: insights from ADRB2 gene polymorphism.
Authors: Olga A. Krasnova; Julia V. Sopova; Anastasiia A. Kovaleva; Polina I. Semenova; Anna S. Zhuk; Daria V. Smirnova; Daria A. Perepletchikova; Vitaly V. Karelkin; Olga M. Lesnyak; Irina E. Neganova
Affiliation: Laboratory of Molecular Science, Institute of Cytology, Russian Academy of Sciences, Saint-Petersburg, Russia
Abstract: Osteoporosis is characterized by increased resorption and decreased bone formation, is pre-dominantly influenced by genetic factors. G-protein coupled receptors (GPCRs) play a vital role in bone homeostasis, and mutations in GPCR genes are associated with osteoporosis. This study aimed to investigate the impact of single nucleotide polymorphism (SNP) rs1042713 in the ADRB2 gene, encoding the beta-2-adrenergic receptor, on osteoblastogenesis. In this study, using quantitative polymerase chain reaction, western immunoblotting, immunofluorescence assays, and flow cytometry, we examined the expression of ADRB2 and markers of bone matrix synthe-sis in mesenchymal stem cells (MSC) derived from osteoporosis patient (OP-MSCs) carrying ADRB2 SNP in comparison with MSCs from healthy donor (HD-MSCs). Results showed signifi-cantly reduced ADRB2 expression in OP-MSCs at both mRNA and protein levels, alongside de-creased TYPE 1 COLLAGEN expression, a key bone matrix component. Notably, OP-MSCs ex-hibited increased ERK kinase expression during differentiation, indicating sustained cell cycle progression unlike to HD-MSC. These results provide novel insights into the association of ADRB2 gene polymorphisms with osteogenic differentiation. The preserved proliferative activity of OP-MSCs with rs1042713 in ADRB2 contributes to their inability to undergo effective osteo-genic differentiation. This research suggests that targeting genetic factors may offer new thera-peutic strategies to mitigate osteoporosis progression.

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